The research is, at present, focused on the relative roles of metabolic activation and detoxification in determining both mutagenic and carcinogenic potential of aromatic amines and amides. Two distinct phenotypes, slow and fast metabolizers, were observed for both metabolic activation and detoxification of the model chemical carcinogen, 2-actylaminofluorene (AAF), in the human liver microsomes from 28 individuals. We observed that individuals who were fast activators of the carcinogen were, in most cases, also fast detoxifiers of the chemical. However, different phenotype patterns exist suggesting that fast activators of a toxin need not also be phenotyped as fast detoxifiers. The activation of the amino acid pyrolysate Trp-P-2 to a mutagen by the same human liver samples was also polymorphic and there was a highly significant correlation between the N-hydroxylation of AAF and the mutagenicity of Trp-P-2. There was no correlation between the N-hydroxylation of AAF and 4-hydroxylation of debrisoquine in these human samples.